What, if any, is the homeostatic control of central venous pressure? Our objectives are: 1. To quantitate the neurogenic venoconstriction which is engendered by hemorrhage or hypoxemia. 2. To evaluate the magnitude, if any, of myogenic venoconstriction, i.e., decreased volume with increased transmural pressure. 3. To quantitate, both in amplitude and time, other short-term mechanisms which act to maintain an adequate filling pressure to the heart, such as passive recoil, collapse, reduced pressure drop with reduced cardiac output (i.e., venous return), stress relaxation and plastic creep, horomonally induced venoconstriction, and transcapillary fluid shifts. 4. To investigate degeneration of compensatory responses when hemorrhagic hypotension is prolonged, i.e., the role in "irreversible" shock. 5. To simulate the essential features of: a. The cardiovascular system to include the homeostatic mechanisms acting to maintain filling pressure of the heart. b. Peripheral microvascular beds to permit estimation of changes in venular and small vein pressure-volume relationships in response to general hemorrhage, hypoxia, and sympathetic nervous system activity.